These St3gal3 knock-out mice may be useful for studies related to epilepsy and inflammation.
Jamey D Marth, Burnham Inst at Univ Calif Santa Barbara
Mice homozygous for this targeted mutation frequently develop neurological symptoms of spontaneous non-lethal epileptic seizures, dermatitis, and failure-to-thrive.
A targeting vector was used to place a floxed neomycin-thymidine kinase expression cassette downstream of the exon encoding the transmembrane domain and a loxP site upstream of the exon. The construct was electroporated into (129X1/SvJ x 129S1/Sv)F1-Kitl +-derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were transfected with a Cre expression plasmid to excise the floxed regions. Gancyclovir-resistant ES cells were injected into blastocysts. Heterozygotes were crossed with ZP3-Cre transgenic mates to produce the recombined and deleted Type 1 allele in the germline. This strain was backcrossed with C57BL/6 mates by the donating laboratory at least nine times.
|Allele Name||targeted mutation 1, Jamey Marth|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||St3gal3, ST3 beta-galactoside alpha-2,3-sialyltransferase 3|
|Strain of Origin||Not Specified|
|Molecular Note||The exon encoding the transmembrane domain was replaced with a single loxP site after the insertion of loxP sites and subsequent expression of cre recombinase in ES cells.|
|Mutations Made By|| |
Jamey Marth, Burnham Inst at Univ Calif Santa Barbara
When maintained as a live colony, heterozygous crosses may be used. Homozygotes develop epilepsy and inflammation of the skin.
When using the ST3Gal-III KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #006899 in your Materials and Methods section.